Garca, E. We also are performing standard PCR, real-time quantitative PCR and genotyping on maternal venous blood and on cord blood, and serological examinations on siblings. Data are managed by a Data Center in Montevideo, Uruguay. Data are entered online at the sites in an OpenClinica data management system, and digital pictures of data forms are sent to the Data Center for quality control. Weekly reports allow for rapid feedback to the sites. Trial registration Observational study with ClinicalTrials.gov Identifier “type”:”clinical-trial”,”attrs”:”text”:”NCT01787968″,”term_id”:”NCT01787968″NCT01787968 to their fetuses . Mother-to-child transmission of has all Rabbit Polyclonal to 5-HT-3A the characteristics required to be a public health priority, as it is relatively frequent, severe, identifiable, and treatable . In reality, it is a neglected disease and a missed opportunity. Therefore, it is urgent to better understand the epidemiology of mother-to-child transmission and to develop effective prevention programs. has been divided into Discrete Typing Units (DTUs): I (TcI) and Non-TcI (II-VI). In humans, TcI is predominant in Mexico and Central America, while Non-TcI is predominant in most of South America, including Argentina . In recent studies from Argentina, the risk of congenital transmission has been estimated to vary between 2.6% and 7.9% [5-8]. By contrast, we know very little about the congenital transmission of TcI. It has been suggested that congenital transmission of is strain related [2,9], and there is an urgent need to know if TcI transmits differently than Non-TcI. Our primary hypothesis is that congenital Staurosporine transmission rates are different for TcI versus Non-TcI. infected women living in regions where TcI is predominant could differ Staurosporine in terms of risk factors for transmitting to their offspring. Low maternal age, low parity, HIV/AIDS, exposure to vectors and high parasitic load have been reported as risk factors for congenital infection [9-14]. Family clustering has been observed in Argentina , suggesting that some mothers might be predisposed to transmit repeatedly. There is limited information about the perinatal outcomes of infected infants in low endemicity areas. Congenital infection has been associated with premature rupture of the membranes and preterm births, in addition to neonatal complications . Further studies are needed to document the impact of infection on perinatal outcomes. The specific aims of this study are: C?1. To determine the rate of congenital transmission of TcI compared to Non-TcI; C?2. To compare the infected mothers characteristics and exposure to vectors in regions where TcI is predominant and regions where Non-TcI is predominant; and C?3. To describe the birth outcomes of infected and uninfected infants born to Staurosporine TcI and Non-TcI seropositive women. Methods/design Overview We are conducting a prospective study in Mexico, Honduras, and Argentina. We are enrolling women at delivery, collecting umbilical cord blood to measure antibodies of maternal origin, and examining and following up the infants of seropositive mothers and siblings (Figure?1). Open in a separate window Figure 1 Study design. At the time of delivery and as soon as possible thereafter, umbilical cord venous blood is collected for all deliveries during the time periods selected for the study. Written informed consent is obtained immediately after delivery (informed consent during labor and delivery is not ethically acceptable). If the woman declines to participate, the cord blood sample is discarded, and no data are recorded. If the woman accepts to participate, we are measuring transmitted maternal antibodies by performing two rapid tests in cord blood (Stat-Pak, Chembio, Medford, New York, and Trypanosoma Detect, InBios, Seattle, Washington). If at least one of the results is positive, we are identifying infants who are congenitally infected by performing parasitological examinations on cord blood and at 4C8 weeks, and serological follow-up at 10 months. Serological confirmation by recombinant ELISA (Wiener, Rosario, Argentina) is performed in cord and maternal blood, and at Staurosporine 10 months. We will perform PCR followed by a qPCR and genotyping Staurosporine on the blood of infected mothers and on the umbilical cord blood. Variables The exposure to TcI will be defined by genotyping showing TcI on maternal blood and/or cord blood. In the absence of successful genotyping on maternal or cord blood, births occurring in Mexico or Honduras will be considered exposed to TcI. The exposure to Non-TcI will be defined by genotyping showing Non-TcI on maternal blood and/or cord blood. In the absence of successful genotyping on maternal or cord blood, births occurring in Argentina will be considered exposed to Non-TcI. The exposure to both TcI and Non-TcI (co-infection) will be defined by genotyping of.